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In this study, the researchers found that treatment with the JAK inhibitor tofacitinib in alopecia areata patients may reduce clonal CD8+ T cell expansions but does not eliminate them entirely, which could contribute to disease relapse.

This study describes a new mouse model for vitiligo that mimics key clinical features such as skin depigmentation and CD8 + T cell infiltration, providing a useful tool for in-depth research and drug discovery.

This study suggests that hypersensitivity and increased serum IgE levels might contribute to the pathogenesis of diffuse alopecia areata through intense local inflammatory infiltration.

This study suggests that SOCS3 treatment may effectively inhibit alopecia areata by suppressing CD8+ T cell activity and IFN-γ production.

This review discusses the bidirectional interactions between human mast cells and CD8 T cells in the skin, particularly in the context of disorders like psoriasis, atopic dermatitis, and vitiligo, and reports no new findings.

In this study using the C3H/HeJ mouse model of alopecia areata, researchers found that hyperexpanded CD8⁺ T cell clones were sufficient to initiate disease, establishing a causal link between T cell clonality and pathogenicity.

In this study, researchers observed significantly higher CD8+ T cell levels in Iraqi patients with Alopecia areata compared to healthy controls, alongside concluding that the condition is more prevalent in men.

This study found that in alopecia areata, treatment with the oral JAK-inhibitor tofacitinib decreased clonally expanded CD8⁺ T cells in the scalp, but many expanded clones did not completely disappear, potentially leading to relapse after stopping treatment.

This study found that in mice with alopecia areata, CD8+ T cells showed clonal expansion and specific regulatory networks, which might help identify new therapeutic targets for patients not responding to JAK inhibitors.

This study in a murine model of alopecia areata found that IFNg is crucial while perforin is not necessary for CD8 T cell-mediated disease development.

Certain CD8+ T cells attack hair follicles in alopecia areata, suggesting they could be targeted for treatment.

In this study, researchers observed elevated levels of epidermal γδ T cells, keratinocytes, and an upregulation of the BST2 gene among immune cells in C3H/HeJ mice with alopecia areata, suggesting a potential role in disease pathogenesis.

This study found that in alopecia areata, epidermal γδ T cells and macrophages contribute to the disease alongside CD8 T cells, with the expression of BST2 marking interferon-driven immune activation in both mouse and human skin, which decreases following treatment with the JAK inhibitor tofacitinib.

This study found that NK and CD8+ T cell infiltration may drive inflammation in androgenetic alopecia, suggesting that targeting IL-15 signaling could offer a new therapeutic approach for hair regeneration.

Expanding regulatory T cells may help treat alopecia areata by reducing harmful immune cells.

This study found that Baricitinib significantly reduced hair loss and immune response in a mouse model of alopecia areata.

In this study of C3H/HeJ mice, researchers observed that alopecia areata is associated with the expansion of exhausted-memory CD8 T cells in multiple organs, with autoreactive activation not fully explained by known mechanisms, shedding light on the immunological dynamics underlying the condition.

This study observed two distinct groups of alopecia areata lesions based on PD-1 expression in T cells from biopsied skin samples, suggesting potential differences in subtypes or stages of the disease that warrant further investigation.

This study found that in biopsied skin samples of alopecia areata, a lower anagen/telogen ratio was associated with increased T cell infiltration, and enhancing the PD-1/PD-L1 axis may inhibit CD8+T cell infiltration and improve the condition.

This study found that phosphodiesterase inhibitors may suppress the proliferation of benign prostatic hyperplasia epithelial cells by modulating CCL5 levels in low androgen conditions.

In this study, treatment with a 5a-reductase inhibitor increased CD8+ T cell infiltration in benign prostatic hyperplasia tissues, suggesting an impact on inflammatory responses.

This research explored the roles of various T cell types in chronic alopecia areata, finding that increased severity of lesions and hair loss may be linked to decreased lesional Foxp3+ Tregs, with a notable role for IL-17 and Th17 lymphocytes in the pathological process.

This study found that mouse skin CD4(+) memory T cells are in equilibrium with the circulation under steady state but increase in specific clusters in response to infection or inflammation.

In this study, blocking the CXCR3 receptor in mice prevented the development of alopecia areata by inhibiting the accumulation of specific T cells in the skin, suggesting a potential therapeutic approach for humans.

This study found that antroquinonol inhibited CD8+ T cell proliferation and reduced proinflammatory cytokine secretion in vitro, while also ameliorating H2O2-induced depigmentation and resisting reductions in hair follicle length, skin thickness, and tyrosinase expression in mice.

This paper proposes that the induction of HF-specific neo-antigens by peripheral CD8+ T cells may maintain self-tolerance but could also lead to immunopathology in conditions like alopecia areata.

This study found that B6.CD80CD86−/− mice developed autoimmune-like alopecia with nearly 100% incidence by 40 weeks, making them a promising model for studying human alopecia areata.

This case study suggests that autoimmunity involving cytotoxic CD8+ T cells may link alopecia areata and human T-cell lymphotropic virus-1-associated myelopathy in adult T-cell leukemia/lymphoma patients.